Effect of hyperbaric oxygen exposure on oxygen tension within the medullary canal in the rabbit tibial osteomyelitis model

Authors

  • Dr. John L. Esterhai Jr.,

    Corresponding author
    1. Department of Orthopaedic Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    • Hospital of the University of Pennsylvania, Second Floor Silverstein Pavilion, 3400 Spruce Street. Philadelphia, PA 19104, U.S.A.
    Search for more papers by this author
  • James M. Clark,

    1. Department of Pharmacology, Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    Search for more papers by this author
  • Harry E. Morton,

    1. Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    Search for more papers by this author
  • David W. Smith,

    1. McKay Laboratory of Orthopaedic Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    Search for more papers by this author
  • Andrew Steinbach,

    1. McKay Laboratory of Orthopaedic Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    Search for more papers by this author
  • Susan D. Richter

    1. McKay Laboratory of Orthopaedic Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
    Search for more papers by this author

Abstract

The effect on intramedullary oxygen tension of 100% oxygen exposure at 1, 2, 2.4, and 3 atm pressure was studied in 12 New Zealand white rabbits with chronic right tibial osteomyelitis. The model, modified from that described by others, incorporates a multipuncture silastic closure plug placed transcortically in the proximal tibial metaphysis through which platinum needle, polarographic electrode oxygen tension determinations can be made without repeat surgical exposure. In 40% of the control, left, noninfected tibial metaphyses the baseline oxygen tension with the animals breathing room air at sea level was suboptimal for leukocyte bacterial killing. This oxygen tension was depressed further in the infected right tibia. Medullary canal oxygen tension increased in response to hyperbaric oxygen exposure in both the infected and noninfected tibiae. Whereas the amount of the oxygen tension increase varied with the presence of infection and depth of dive, neither the time for oxygen tension to plateau nor the time required for return to baseline tension after completion of hyperbaric oxygen exposure varied with the presence of infection or depth of dive. After completion of hyperbaric oxygen exposure, the oxygen tension within the medullary canal returned to baseline within 15 min.

Ancillary